Inhibition of non-homologous end joining repair impairs pancreatic cancer growth and enhances radiation response - Wikidata - wikimedia - TriplyDB

Inhibition of non-homologous end joining repair impairs pancreatic cancer growth and enhances radiation response

Inhibition of non-homologous end joining repair impairs pancreatic cancer growth and enhances radiation response

http://www.wikidata.org/entity/Q28728326

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DNA repair targeted therapy: The past or future of cancer treatment?Chemotherapeutic compounds targeting the DNA double-strand break repair pathways: the good, the bad, and the promising Perspectives on the combination of radiotherapy and targeted therapy with DNA repair inhibitors in the treatment of pancreatic cancer Preventing Damage Limitation: Targeting DNA-PKcs and DNA Double-Strand Break Repair Pathways for Ovarian Cancer Therapy miR-155 Overexpression Promotes Genomic Instability by Reducing High-fidelity Polymerase Delta Expression and Activating Error-Prone DSB Repair Wwox-Brca1 interaction: role in DNA repair pathway choice The Effect of VPA on Increasing Radiosensitivity in Osteosarcoma Cells and Primary-Culture Cells from Chemical Carcinogen-Induced Breast Cancer in Rats.The complex landscape of pancreatic cancer metabolism Targeting DNA repair pathways for cancer treatment: what's new?Novel role for non-homologous end joining in the formation of double minutes in methotrexate-resistant colon cancer cells.Caveolin-1 is Associated with Tumor Progression and Confers a Multi-Modality Resistance Phenotype in Pancreatic Cancer.DNA-Dependent Protein Kinase As Molecular Target for Radiosensitization of Neuroblastoma Cells.PARI overexpression promotes genomic instability and pancreatic tumorigenesis.Triapine potentiates platinum-based combination therapy by disruption of homologous recombination repair.Key clinical beam parameters for nanoparticle-mediated radiation dose amplification.MUC1-mediated metabolic alterations regulate response to radiotherapy in pancreatic cancer.DNA repair of myeloma plasma cells correlates with clinical outcome: the effect of the nonhomologous end-joining inhibitor SCR7.Combining carbon ion irradiation and non-homologous end-joining repair inhibitor NU7026 efficiently kills cancer cells.Biological determinants of radioresistance and their remediation in pancreatic cancer.Sulforaphane enhances irradiation effects in terms of perturbed cell cycle progression and increased DNA damage in pancreatic cancer cells.Radiation Treatment in Women with Ovarian Cancer: Past, Present, and Future Phytotherapeutics Oridonin and Ponicidin show Additive Effects Combined with Irradiation in Pancreatic Cancer in Vitro.

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P2860

Inhibition of non-homologous end joining repair impairs pancreatic cancer growth and enhances radiation response

http://www.wikidata.org/entity/Q28728326

description

2012 nî lūn-bûn

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Inhibition of non-homologous e ...... nd enhances radiation response

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Inhibition of non-homologous e ...... nd enhances radiation response

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Inhibition of non-homologous e ...... nd enhances radiation response

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Alec C Kimmelman

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Dipanjan Chowdhury

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Dong-Hyun Lee

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Xiaoxu Wang

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Ying-Hua Li

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Yunfeng Pan

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P2860

The mechanism of double-strand DNA break repair by the nonhomologous DNA end-joining pathway

Hallmarks of Cancer: The Next Generation

DNA damage triggers a prolonged p53-dependent G1 arrest and long-term induction of Cip1 in normal human fibroblasts

DPC4 gene status of the primary carcinoma correlates with patterns of failure in patients with pancreatic cancer.

Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy

Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase

A critical role for histone H2AX in recruitment of repair factors to nuclear foci after DNA damage

Up-regulation of DNA-dependent protein kinase correlates with radiation resistance in oral squamous cell carcinoma

A novel DNA-dependent protein kinase inhibitor, NU7026, potentiates the cytotoxicity of topoisomerase II poisons used in the treatment of leukemia

Regulation of DNA double-strand break repair pathway choice

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